Neurosurgery notes/Injury classification of peripheral nerve

Injury classification of peripheral nerve

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Peripheral nerve injuries
RAG
RAG

Grading summary

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Seddon
Conduction velocity
MUAPs
CMAPs
SNAPs
To be aware
Neuropraxia
Maintained
None
Normal, slight reduction proximally
Reduced
Permanent conduction slowing due to thinner internodes
Axonotmesis
Reduced
None
Reduced proportional to axonal loss
Reduced
Positive sharp waves and fibrillations
Neurotmesis
Nil
None
Reduced proportional to axonal loss
Absent
Positive sharp waves and fibrillations
Seddon
Sunderland
Pathology dfn
Wallerian degeneration
NCS
Spontaneous recovery
Neuropraxia
I
Intact basement membrane (physiologic rather than anatomic transection/nerve in continuity)
No (maybe just focal demyelinating injury)
No conduction across lesion. Conduction prox. + dist. to lesion
Complete (in h/mo; ave: 6–8 wk)
Axonotmesis
II
Complete interruption of axons—myelin sheaths with intact endoneurium
Yes (dist. to injr)
Block distally
Good
Axonotmesis
III
Axons + endoneurium disrupted with intact perineurium
Yes (dist. to injr)
Block distally
Variable (possibility of scarring)
Axonotmesis
IV
Axons + endoneurium + perineurium disrupted with intact epineurium
Yes (dist. to injr)
Block distally
Poor, neuroma formation
Neurotmesis
V
Complete transection (loss of continuity)
Yes (dist. to injr)
Block distally
NO
  • Pure grades of injury rarely exist; severity of most injury occurs along a continuum.

Class I

  • Neuropraxia
    • Interruption of conduction without loss of axonal continuity and preserved supportive structures.
    • Prognosis: normally rapid and complete (days, weeks).

Class II

  • Axonotmesis
    • Disruption of axonal continuity and its myelin with intact endoneurium.
    • Prognosis: variable, generally good, with worse prognosis for proximal injuries and injuries that do not re-implant in the muscle.

Class III

  • Neurotmesis
    • Disruption of all nerve layers. Recovery is not possible without appropriate surgical intervention. It is a total severance or disruption of the entire nerve.
    • Prognosis: poor especially without intervention; normally incomplete.

Clinical

  • Nerve injuries (Seddon Classification)
      • Features
      Neuropraxia
      Axonotmesis
      Neurotmesis
      Mechanism of injury
      • Pressure on a nerve → local ischaemia
      • 30mmHg can cause paresthesias
      • Increased latencies
      • 60mmHg can cause complete block of conduction
      • Chronic compression leads to Schwann cell apoptosis
      • Stretched a nerve → Wallerian degeneration of nerve
      • 8% elongation reduces microcirculation
      • 15% elongation disrupt axons
      • Division of a nerve → Wallerian degeneration
      Myelin Sheath
      Damaged
      Damaged
      Damaged
      Axon
      Intact
      Damaged
      Damaged
      Schwann cell and connective tissue
      Intact
      Intact (this allow for some recovery )
      Damaged
      Electrophysiologic studies
      Nerve conduction velocity slowing or
      a complete conduction block
      no fibrillation potentials
      Fibrillations and positive sharp waves on EMG
      Fibrillations and positive sharp waves on EMG
      Prognosis
      Full recovery
      Unpredictable recovery
      • No recovery unless surgical repair performed
      • Neuroma formation at proximal nerve end may lead to chronic pain
      Examples
      Nerve root compression in disc
      Brachial plexus stretch injury Suprascapular nerve stretching injuries in volleyball players
    • If the gap between the two cut ends in neurotmesis is more, the growing axonal buds get mixed up with connective tissue to form a mass called a neuroma.
    • Regeneration process after transection
      • Distal segment undergoes Wallerian degeneration (axoplasm and myelin are degraded by phagocytes)
      • Existing Schwann cells proliferate and line endoneurial basement membrane
      • Proximal budding (occurs after 1 month) leads to sprouting axons that migrate at 1mm/day to connect to the distal tube
    • Variables affecting regeneration
      • Contact guidance with attraction to the basal lamina of the Schwann cell
      • Neurotropism
      • Neurotrophic factors (factors enhancing growth and preferential attraction to other nerves rather than other tissues)
    • Functional recovery during regeneration (in order)
      • Sympathetic activity
      • Pain
      • Temperature sensation
      • Touch
      • Proprioception
      • Motor function
      • Motor function is the first to be lost and the last to recover

Three methods of neuronal plasticity

  • Sprouting proximal to the injury
  • Sprouting distal to the injury
  • Strengthening of synapses

Axon regeneration

  • Adhesion complex: integrin ligand (tenascin)
    • Inc. expression in inflammation
    • Dec. expression at maturation
  • Need to also stimulate axonal transport of growth protein into the axon

Plasticity

  • Critical period of plasticity : 1.5 - 5 yrs
  • How to turn on plasticity
    • Chondrotinase remove proteoglycan chain that prevent neuroplasticity → stimulate sprouting
    • Sulfation of proteoglycans stops plasticity
    • Perineural nets has chondroitin sulfate → inhibit plasticity
  • Will also require targeted rehab to help the body focus on regenerating specific targeted connections. Otherwise other connection will compete and inhibit desired connection

Images

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